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T-LYMPHOCYTES CONTRIBUTES TO MORTALITY AND IMMUNOSUPPRESSION IN SEPSIS
1 Surgery, Rhode Island Hospital, Providence, Rhode Island, United States
2 surgery, Rhode Island Hospital, Providence, Rhode Island, United States
* To whom correspondence should be addressed. E-mail: aayala{at}lifespan.org.
Studies have indicated that 
T-lymphocytes play an important role in the regulation of immune function and the clearance of intracellular pathogens. We have recently reported that intraepithelial lymphocytes (IEL), which is rich in T-cells, within the small intestine illustrated a significant increase in apoptosis and immune dysfunction in mice subjected to sepsis. However, the contribution of T-cells to the host response to polymicrobial sepsis remains unclear. In this study, we initially observed that following sepsis induced by cecal ligation and puncture (CLP) there was an increase in small intestinal IEL CD8+-+ T-cells in control +/+ mice. Importantly, we found an increased early mortality in mice lacking T-cells (-/-) after sepsis. This was associated with a decrease in plasma TNF-
, IL-6 and IL-12 levels in -/- mice compared to +/+ mice after sepsis. In addition, even though in vitro LPS-stimulated peritoneal macrophages showed a reduction in IL-6 and IL-12 release after CLP, these cytokines were less suppressed in macrophages isolated from -/- mice. Alternatively, IL-10 release was not different between septic +/+ and -/- mice. While Th1 cytokine release by anti-CD3-stimulated splenocytes was significantly depressed in septic +/+ mice, there was no such depression in -/- mice. However, T-cell deficiency had no effect on Th2 cytokine release. These findings suggest that T-cells may play a critical role in regulating the host immune response and survival to sepsis, in part by alteration of the level of IEL CD8+-+ T-cells and through the development of Th1 response.
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